Abstract 148: TCD Monitoring during Intrathecal Nicardipine Use in Aneurysmal Subarachnoid Hemorrhage Induced Vasospasm

Introduction/Purpose Subarachnoid hemorrhage secondary to a ruptured cerebral aneurysm can be a devastating disease process with high rates of morbidity and mortality. For those who survive the initial hemorrhage, secondary delayed cerebral ischemia is the highest cause of further neurologic injury. The current standard of care is regular transcranial doppler (TCD) monitoring to evaluate for cerebral vasospasm and common interventions include intraarterial pharmacologic vasodilation with verapamil or nicardipine and balloon or stent‐assisted angioplasty in refractory cases. Intraventricular nicardipine (IVN) can also be used as rescue therapy for patients with treatment‐refractory cerebral vasospasm, and has been shown to decrease the rates of escalation to more invasive rescue interventions such as angioplasty and decrease the incidence of delayed cerebral ischemia. Methods We present a case of aneurysmal subarachnoid hemorrhage induced vasospasm who had drastic improvement in TCD mean velocities and subsequent good clinical outcome after receiving courses of IVN without developing intraventricular infectious complications. Results A 53‐year‐old female presented with “worst headache of her life.” CT Brain showed basal cistern subarachnoid hemorrhage with interventricular hemorrhage in the 4 th ventricle. Emergent diagnostic cerebral angiogram (DCA) showed a right posterior communicating artery aneurysm (6.68 mm x 2.52 mm x 2.80 mm) with a neck of 2.25 mm and patient underwent successful trans‐arterial coil embolization with small residual neck (Raymond Roy class II). Patient was admitted to neurosurgical intensive care unit for continued management and initially placed on oral nimodipine but did not remain on this therapy due to hypotension and vasopressor requirement. Initial MRI brain showed scattered embolic and watershed infarcts with MRA brain showing concern for severe vasospasm involving the middle segment arteries of the bilateral anterior circulation. TCD monitoring showed concern for progressive worsening velocities more so in posterior circulation, and follow‐up DCA showed multifocal stenosis consistent with vasospasm. Following intraarterial verapamil infusion, there was mild improvement in the non‐flow limiting moderate stenosis within the right middle cerebral, left anterior cerebral, and basilar arteries. Given patient inability to remain on oral nimodipine for systemic blood pressure goals, intraventricular nicardipine 4mg q8h was started for approximately a 3‐day course. Repeat TCD mean velocities after just two doses of IVN showed drastic reduction and improvement. Two days later, a repeat DCA was negative for vasospasm. Approximately two days after IVN treatment was stopped, patient once more had TCD velocities with multifocal definite vasospasm, and a repeat 3‐day course of IVN was initiated with complete resolution of vasospasm. The patient was unable to tolerate external ventricular drainage clamp trials and ventriculo‐peritoneal shunt was placed without complications. She was ultimately discharged to inpatient rehabilitation in good condition with some residual aphasia and weakness. Conclusion In cases of aneurysmal subarachnoid hemorrhage induced vasospasm, intraventricular nicardipine can be an effective potential treatment option that has been shown to reduce the incidence of delayed cerebral ischemia. IVN can be especially considered in patients with refractory vasospasm who cannot otherwise tolerate oral nimodipine or repeated endovascular therapies.